Thursday, June 29, 2006

Here is the discussion I have been edited for the BSA between Mark Onslow and Scott Yaruss: see here.

Mark,The diagnosogenic theory stated that stuttering was caused, in part, by parents inappropriately drawing attention to a child’s otherwise normal disfluencies. In recent years, many have commented on the numerous shortcomings of this theory as an explanation for early stuttering, and, in particular, on the negative effects it has had on treatment planning and clinical decision making.

Given your recent research on stuttering treatment, combined with research on early recovery, with what theoretical framework would you replace the diagnosogenic theory, and how would such a theory help to explain basic phenomena associated with childhood stuttering?

Scott,There should currently be no replacement for the diagnosogenic theory as a driver of treatment for early stuttering. Many theories are available (for an overview, see Packman & Attanasio, 2004), but none of them has proven to be correct, and only one of them—or perhaps none of them—is correct. Hence for the time being, it is a dubious practice to base treatment on any theory of what causes or perpetuates stuttering.

We are all desperate to find out what causes stuttering. But intervention of early stuttering can occur independent of efforts to uncover its cause. For example, the Lidcombe Program is not driven by a theory of the cause of stuttering, and is nonetheless efficacious according to a recently published randomised controlled trial (Jones et al., 2005).

Mark,

Few would doubt the efficacy of the Lidcombe program, as described in numerous publications and the recent clinical trials. Still, some may question its effectiveness in daily clinical settings. Further, is Lidcombe the only way to accomplish our common goal of eliminating stuttering in young children?

Of course, it is true that theory has not always served our field well. Many clinicians still cling to ineffective treatments derived from the long-disproved diagnosogenic theory, but would this necessarily have to be the case with other theories?

Improvements in treatment might still be achieved through the rigorous application of theory-driven clinical research aimed at uncovering factors involved in the onset, development, and maintenance of the disorder. Uni-dimensional theories have proven unsatisfactory throughout the history of our field, so I would start with a theory that incorporates more than one factor as a potential cause for stuttering.

Scott,I hope that no clinician is still using the diagnosogenic theory to treat stuttering. For example, Bloodstein tried for years to implement the treatment suggested by the theory, but failed completely (see Bloodstein, 1986). I do not think my concerns are an overstatement. A theory of the cause and development of stuttering would certainly be fine as a basis for treatment as you say, but with two provisos. First, the theory is verified with the scientific method. Second, the treatment based on the theory is evaluated with clinical trials of an acceptable standard. Surely it is unethical to provide health care with unproven treatments? The local doctor would not do it for asthma, and neither should the local speech pathologist do it for early stuttering.

Yes, the effectiveness of the Lidcombe program at the population level is not yet well researched. Also, it may not be the only way to treat early stuttering. There might well be other treatments, and I look forward to the publication of clinical trials of other treatments. If clinical trials show that there is a better and quicker treatment, I will be the first to use and endorse it.

However, I would not endorse multifactorial theory of stuttering as a source of treatment development. First, multifactorial theories of stuttering are completely and irretrievably wrong from empirical and logical perspectives. Second, no clinical trial shows the capacity of multifactorial treatments to control stuttering. There is a real risk that the errors of the diagnosogenic era will be repeated if we use multifactorial theories to treat children: that we will think that we know the cause of stuttering when we do not, and that we know what is an efficacious treatment for early stuttering when we do not.

I also do not agree with your claim that one type of theory, such as multifactorial theory, has been more successful than another such as single factor theory. In fact, no theory has been successful in explaining the cause of stuttering (see Packman & Attanasio, 2004).

Sunday, June 25, 2006

At conferences, I sometimes hear people proclaiming that stuttering has been a gift and inspiration to them. The process of overcoming stuttering has made them stronger and wiser human beings. Indirectly they thereby question my "obsession" with understanding stuttering. Yet others tell me that they are not the least interested why they stutter. Their rationale is: "I stutter. I have no idea why. Why waste time thinking about the why. I will concentrate on what I do now and try to reduce my stuttering." Again, they are no interested in research.

I never quite knew how to reply, as they are not completely wrong, though I felt they were somewhat on the wrong track. Now I have a clear reply: "Yes, overcoming or reducing stuttering makes you a stronger and wiser person. Attending self-help groups, self-reflecting, and doing a therapy makes you grow as a person. And there is no need to understand stuttering and its causes or mechanism. Following an established therapy is sufficient to become more fluent. But, let's go to a 4-year old child. Are you going to tell that child: Dont worry if you stutter, once you have overcome stuttering (after 20 years of pain, despair, and embarrassment), you are a stronger person? Or are you telling him/her that we dont have more effective way to reduce his/her stuttering because you are not interested in understanding stuttering better as it was not important for you personally?"

Thursday, June 22, 2006

I hate the analogy of comparing stuttering to an addiction. I know various people use it, but if stuttering is caused by a difficulty, say in the basal ganglia, that is to some degree out of the control of the person who stutters, it seems wrong and unfair to encourage punishment for something. I think the comparison of stuttering to something so negative causes so many difficulties, and exacerbates the potential for people to become anxious about their speech as a result of fearing negative evaluation. I prefer analogies where there isn't an implication of fault- for example poor vision- then treatments and strategies are about optimising your abilities (e.g. wearing glassess, doing eye exercises) raher than punishment!

1) I consider most stuttering therapies a behavioural therapy. You need to change your behaviour (the way you speak or stutter). In the short term, behavioural therapies are extremely successful, be it loosing weight, getting off hard drugs like heroin or crack cocaine, stopping smoking, stopping to drink, stay out off crime, and so on. Unfortunately, all these therapies have lousy success rate in the long-term. People in general fall back to their old behaviour, EVEN THOUGH THEY DO NOT WANT TO. We all know that old habits creep in very slowly: "Just a little piece of chocolate", "I am stressed. Oh there is chocolate lying around.", "I am fed up. I on purpose eat chocolate now. I want to punish myself.", or "Great. I have succeeded easting no chocolate anymore. So now, a bit of chocolate is OK." We readily succumb to short-term urges that win out against our long-term goals.

2)I consider that stuttering is based to varying degree on faulty/weak hardware in the brain which kick-starts and feeds the development of secondary symptoms that re-enforce and increase stuttering severity like fear, lack of eye contact, avoidance, tension, and so on. So, we need to undertake a superhuman effort to control our speaking and reduce the secondary symptoms. I also think that a case can be made that all other disorders that are treated with behavioural therapies are also not just bad habits. Being overweight, addicted to drugs, and being criminal are to some degree in our brain in that these people are pre-disposed to such behaviour under the right circumstances. Especially once you are addicted, your brain changes and you absolutely crave for drugs.

3) Bad vision is not a good example, as you do not need to change your behaviour to see better. You should get glasses.

3) I only compare one aspect stuttering to one aspect of addiction, I do not say that we just become to stuttering and that you crave for it as some would like us to to fit their theories. I am talking about the process of getting off stuttering or drugs.

4) When I think about an issue scientifically / intellectually, I do not care what the political implications are or the impact on other people. My mind is not restricted to "political correctness" (what seems wrong to say), so I do wonder why the fastest runners are black, why black kids underperform whereas the Indian minority outperform, why there are so few women in math / science, and why do less women stutter.

5) I am contemplating what is most effective. If it is punishment, so be it. If it is encouragement, so be it.

6) Punishment is not necessarily bad, especially if the person to be punished agrees with it. In a sense, his long-term thinking agrees that his short-term-urges should be punished.

Thursday, June 15, 2006

I have been reading about an therapy against alcohol addiction with an unusually high success rate of 50% after five years. The secret is that the recovering alcoholics take a substance that makes them feel physically sick when drinking alcohol. The substance reacts with alcohol and creates a toxic substance.

Maybe that is what is needed, we need punishment when people start stuttering again, but then again staying fluent after a fluency shaping therapy is about keeping up practise rather than about not stuttering (drinking alcohol) again. But in a sense, relapse happens when someone is not using the new speech technique anymore and using the old one (starts the old habit like drinking again).

But here is another twist. They gave one group of alcoholics a placebo (i.e. a pill containing nothing), and they still showed the high success rate!!!! So in a sense you dont need the drug at all but you need a drug that is able to punish for new stuttering!

Tuesday, June 13, 2006

A reader to this blog sent me an interesting article on the potential for abuse of Pagoclone. The authors are Harriet de Wit, Lisa Vicini, George M. Haig, Thomas Hunt, and Douglas Feltner (Note that some are associated to Pfizer, which is a rival company of Indevus, the producer of Pagoclone, as far as I am aware of). Briefly, they compare Pagoclone to Diazepam (also an anti-anxiety drug). They suggest that Pagoclone is relatively safe to use with some effect on mood, subjective and objective sedation, similar to Diazepam. And a similar (relatively low) potential of abuse. Though the picture may change a bit as the effect is dependent on the actual dosis.

Judge for yourself...

Evaluation of the Abuse Potential of Pagoclone, a Partial GABAA Agonist

This study assessed the abuse potential of pagoclone, a partial agonist at the g-aminobutyric acid type A (GABAA) benzodiazepine receptor site, in healthy recreational drug users. Twenty-three young adults, who reported past recreational use of sedative drugs or alcohol, participated in 4 sessions during which capsules containing pagoclone (doses: 1.2 mg, the higher end of the proposed therapeutic dose range, and 4.8 mg, a 4-fold higher dose), diazepam (dose, 30 mg), or placebo were randomly administered under double-blind conditions. Subjective ratings of mood, drug effects, and psychomotor tests were completed at regular intervals after ingesting the capsules. On most of the standardized measures of abuse potential, pagoclone (dose, 4.8 mg) was rated as being similar to diazepam. Both drugs increased the ratings of good effects and drug liking. However, pagoclone also produced some adverse mood effects that might limit its potential to be used recreationally, and it produced fewer sedativelike effects on some measures. In general, the results with these doses indicate that the abuse potential of pagoclone is similar to that of diazepam, although its profile as a partial agonist suggests that differences between the drugs may emerge at higher doses.

( from Journal of Clinical Psychopharmacology Volume 26, Number 3, June 2006)

Friday, June 09, 2006

I met up with Carl and Lloyd on Wednesday afternoon at the Metropolitan in New York, and we went to a near-by cafe. It was good to hear that they both enjoy reading my blog.

The discussion was also an interesting one. I was sitting opposite the two, and both are currently in treatment for their stuttering. Carl has done the McGuire course, which is a behavioural theory with coastal breathing being a core technique, and Lloyd took part in the Pagoclone study and is now in an one year open-label extension. Carl, a tidier and more intellectual version of Frank Zappa :-), spoke about how the course has changed his outlook, and about the intense experience that he felt when realising that he could control his stuttering more and the importance of will power. He got a bit over excited about the paradox of completely believing that this is the right way to become more fluent and not being dogmatic that this should help everyone else. I think it is fair to say than neither myself, Lloyd, nor himself did fully understand what he meant! I am sure he will give us a more collected summary of his thoughts here. Carl said that he was a mild to medium severe stutterer, but that he is pretty fluent at the moment. And I have to agree with him. Apart from some coastal breathing, he spoke completely naturally.

Lloyd spoke about his experiences on Pagoclone, and one thing is clear: Pagoclone is no wonder drug. He still has clear blocks and prolongations. On the other hand, I did feel that his stuttering symptoms were clearly visible but of low intensity, a bit like people doing van Ripper. He did not seem to struggle a lot and seemed patiently going through the blocks and prolongations. Now I dont know how he spoke before the trials. Lloyd said that he felt in greater control of his speech, but only after taking the high dose. He also said that family members thought he spoke better on the phone. So his stuttering seemed to have gotten easier, but no cure. I forgot to ask him whether he wants to write a post about his experience, but will do so. He also mentioned that his recordings were probably more positive due to them being taken in a calm room with a nice female speech therapist!

We also discussed whether a combination of a behavioural therapy and medication would be useful. And whether medication can improve to such a degree that it makes stutterers fluent. Intuitively, meeting the two has made me think that medication is probably most suited for more severe stutterer to give them break and allow for more behavioural work. Finally, we talked about relapse, which is the real test for any behavioural therapy.

P.S. Just want to say that these are individual cases not necessary a reflection of a wider population.

Tuesday, June 06, 2006

I am in NY, but missed my meeting with Carl and Lloyd (readers of my blog and fellow stutterers). I was on time, but couldnt find the piece of paper where I wrote down the bar we were supposed to meet. But there are so many bars and so on at Central Station... :-(

But was excellent training for maintaining eye contact. I was running for half an hour making eye contact with everyone I possibly could in the hope it would be Carl or Lloyd recognising me from the picture on my blog...

Oh well... maybe we can still meet up.

Talking about eye contact... I have a theory that girls think male stutterers are obsessed by breasts. Why? I am often avoiding eye contact by looking a bit down... of course when I talk to a girl, I happen to look at precisely the place I shouldnt be looking at even though I dont want to look there... what a perfect excuse... oh well... :-)